Augmented skeletal muscle metaboreflex function in hypertensive adults

Recent animal studies have reported that exercise pressor reflex mediated increases in blood pressure are exaggerated in hypertensive (HTN) rodents. Whether these findings can be extended to human hypertension remains unclear. PURPOSE We sought to investigate the metabolic component of the exercise pressor reflex (muscle metaboreflex) in HTN humans. METHODS Mean arterial pressure (MAP), muscle sympathetic nerve activity (MSNA), and metabolites were measured at baseline, during static handgrip (HG) exercise at 30% and 40% maximal voluntary contraction, and during post‐exercise ischemia (PEI) to isolate the muscle metaboreflex in normotensive (NTN; n=23; 60±1 years) and HTN (n=15; 63±1 years) subjects. MAP and MSNA responses were also quantified during a non‐exercise sympatho‐excitatory stimulus (cold pressor test). RESULTS The changes in MAP and MSNA from baseline to PEI were greater in HTN subjects after the 30% HG trial (MAP: NTN, Δ 13±1 vs. HTN, Δ 16±2 mmHg, p=0.05; MSNA: NTN, Δ 54±10 vs. HTN, Δ 101±11 AIU/min, p=0.009) and after the 40% HG trial (MAP: NTN, Δ 15±1 vs. HTN, Δ 22±2 mmHg, p=0.007; MSNA: NTN, Δ 57±10 vs. HTN, Δ 136±11 AIU/min, p≤0.001). There were no group differences in metabolite concentration. MAP and MSNA responses to the cold pressor test were not different between groups. CONCLUSION These data suggest that muscle metaboreflex function is augmented in HTN humans. Supported by HL07485